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P3‐065: Transection of Targeted Axonal Pathways Inhibits Network Spread of Tau Pathology in a P301S Model of TAU Propagation
Author(s) -
Ahmed Zeshan,
Cooper Jane,
Fisher Alice,
Jackson Kate,
Murray Tracey K.,
Cavallini Annalisa,
Bose Suchira,
Goedert Michel,
Hutton Michael,
O'Neill Michael J.
Publication year - 2016
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2016.06.1723
Subject(s) - hippocampus , hippocampal formation , tau protein , tau pathology , tauopathy , pathological , neuroscience , pathology , medicine , psychology , alzheimer's disease , neurodegeneration , disease
classified older individuals into disease stages using deciles of whole-brain PIB distribution volume ratio (DVR), assuming that those with lower whole-brain DVRs are at earlier stages. We identified epicenters by finding ROIs that met the following criteria: (1) the PIB DVR in the ROI is greater than the average of its neighbors on the MST, (2) in the successive stage average PIB DVR in the neighbors increases, and (3) the ROI is not near another epicenter on the MST. Results:At all stages of PIB progression we found a strong significant positive correlation of regional PIB DVR with the average PIB DVR in neighboring regions at the successive stage. Moreover, with each 5 or 10 percentile increase in whole brain DVR we found a progressively stronger positive correlation of regional PIB DVRwith increased PIB DVR in neighboring regions relative to the initial stage. Finally, we identified distinct epicenters of PIB accumulation in the left posterior cingulate, left rostral anterior cingulate, left putamen, right pars opercularis, right suparmarginal, right lateral orbitofrontal, and right pericalcarine cortex which this approach identified as arising independently from one another. Conclusions:PIB appears to arise from multiple epicenters based on patterns of normal brain connectivity.